Recent advances have highlighted the role of specific immune pathways, including Th2 cytokines (IL‐4, IL‐13) and innate immune responses, in driving AD disease progression.[34, 35] Moreover, scRNA‐seq studies have provided unparalleled insights into the cellular and molecular heterogeneity of AD, particularly regarding the interactions between structural and immune cells in lesional tissues.[5, 36, 37] Our findings presented here build on these advancements by identifying PDE4D as a critical regulator of AD pathogenesis and a promising therapeutic target. This evidence concerns the gene IL13 and Alzheimer disease.